About 70% of patients with gout are treated exclusively in the primary care setting. Because the prevalence of gout is rising, particularly among older patients, you are increasingly likely to encounter this disease in your practice.
In a 3-part series of podcasts I recorded for ConsultantLive.com, I discuss how the current understanding of gout is changing and how this affects the management of the disease:
• Part 1 is an overview, in which I describe the pathogenesis of gout and the risk factors for the disease.
• Part 2 focuses on diagnosis; I offer real-world advice about when and how to make a presumptive diagnosis, indications for synovial fluid analysis and other studies, and which disorders to consider in the differential.
• In part 3, I map out the options for relief of acute attacks and for prevention of future ones.
Here I offer some clinical “pearls” from my podcast series.
DIAGNOSTIC PEARLS
Gout results from the deposition of monosodium urate crystals in tissues, which occurs at a serum urate level of at least 6.8 mg/dL. Hyperuricemia in the absence of crystal deposition is not gout.
Clinical pearl No. 1: Asymptomatic hyperuricemia generally does not require treatment; however, there may be circumstances in which urate-lowering therapy is appropriate.
What are the risk factors for gout? Among the factors that predispose patients to this disease are:
• Male sex, although the disease is equally common in postmenopausal women.
• Older age.
• End-stage renal disease.
• Consumption of red meat, organ meat, seafood, and products that contain high-fructose corn syrup.
• High alcohol(Drug information on alcohol) intake, particularly beer.
• Use of drugs such as cyclosporine, thiazide diuretics, and low-dose aspirin(Drug information on aspirin).
• Certain genetic influences, which are not well understood.
In an acute attack of gout, the lower extremities are typically involved. About 80% of initial gout attacks are monarticular, and the first metatarsophalangeal joint is eventually affected in about 90% of patients with gout. Untreated, an attack usually resolves within 3 to 14 days.
To help make a presumptive diagnosis, here are some questions to ask the patient:
• When did the symptoms start? Was the onset sudden?
• Was this the first time you experienced pain or swelling at this joint?
• If not, which other joints have been affected?
• Do you have a fever?
• Do you have relatives with similar complaints?
• Are you taking medications that may contribute to gout, such as thiazide diuretics?
• What have you been eating or drinking recently? How often do you consume red meat, shellfish, and beer?
Clinical pearl No. 2: A clinical diagnosis is usually correct, particularly in a patient who presents with
podagra. But it is not definitive without confirmation of characteristic urate crystals from synovial fluid or
tophi.
TREATMENT PEARLS
The first step in the treatment of gout is lifestyle modification. Diets tailored to insulin resistance and weight reduction are preferable to low-purine diets, which most patients do not find palatable. In my podcast, I discuss the challenges of motivating patients to institute and adhere to dietary changes. Other issues I address are:
• What to consider when selecting an anti-inflammatory agent.
• When to start urate-lowering therapy.
• Whether urate-lowering therapy should be continued during an acute flare.
Finally, I offer these clinical pearls:
No. 3: Reduce serum uric acid levels to less than 6 mg/dL rather than the 6.8 mg/dL saturation level for crystallization. Do not rely on laboratory studies that report normal values as between 6 and 9 mg/dL; these are population levels, not physiologic levels.
No. 4: During initial treatment, when patients may experience flares, counsel patients to maintain the therapeutic regimen. Lifelong urate-lowering therapy is required to sustain the benefits.
No. 5: Hyperuricemia is frequently encountered in patients with metabolic syndrome. Consider the possibility of gout in patients who have this syndrome.
